The Limits of Self-Control: Self-Control, Illusory Control, and Risky Financial Decision Making

Can high self-control have drawbacks? Extensive research has shown the lifelong benefits of self-control for important outcomes such as education, health, income, and happiness. Far less work has been done on its potential negative impacts, where an overwhelmingly positive trait can end up having a less than positive effect on behavior. Recent research suggests that one such side effect may be an increased susceptibility to illusory control (IOC): in situations where actual control is limited but the potential for illusory control is high, high self-controllers may end up being more prone to overconfidence than low self-controllers, and this susceptibility may play out in suboptimal risk-taking behavior. Here, a series of five studies tests this causal chain, exploring the links between self-control and illusory control and the resulting impact of the relationship on risky decisions in the financial domain. In studies 1 and 2, high self-controllers consistently underperformed low self-controllers on two tasks of risk-taking, the Columbia Card Task and the Lottery Gambling Task. These effects persisted both under stress and in normal conditions. Individuals high in self-control failed to learn as well from negative feedback and were more prone to overconfidence, leading us to posit a causal mechanism rooted in the illusion of control, and specifically, in the positive affect that accompanies it. Studies 3 through 5 proceeded to test this relationship directly, on a decision-making task that looked specifically at financial risk-taking, the Behavioral Investment Allocation Strategy (BIAS). Across the three studies, we validated our findings from Studies 1 and 2 in the new risk-taking task, by showing that individuals low in self-control consistently outperformed those in high self-control by making more optimal choices and fewer errors throughout the game. We next tested the precise causal mechanism of the observed decision making patterns by manipulating IOC (Study 3), positive affect (Study 4), and perceived self-control (Study 5). We found that inducing IOC increased the number of errors committed by both high and low self-controllers across the board: individuals in the IOC condition made fewer optimal choices and performed worse overall, confirming our suspicion that IOC can be responsible for sub-optimal choices on financial risk-taking in stochastic environments. However, because the effect was non-selective, the precise causal mechanism and its relations to self-control still remained to be determined. In Studies 4 and 5, we were able to disambiguate the mechanism behind the underperformance caused by IOC. Specifically, we demonstrated that inducing positive affect (Study 4) reduced the number of optimal choices for low self-controllers on the BIAS task, making them look more like high self-controllers in their decisions. Surprisingly, the induction actually improved performance by high self-controllers. The perceived self-control induction (Study 5) also had a differential effect on high and low self-controllers. It decreased the number of optimal choices made by low self-controllers, again making them look more like high-self-controllers--but, just as with the positive affect induction, it increased the number of optimal choices made by high self-controllers. The increase in positive affect that accompanied the self-control induction was a significant mediator of the effect, a mediation that held when we pooled data from all three studies into a single affective mediation analysis. The induction results for low self-controllers confirm our hypothesis that the positive affect that usually accompanies both the illusion of control and high self-control can be an Achilles heel of high self-control in certain environments with limited actual control, creating a feeling of overconfidence that translates into suboptimal decision making. We explain the surprising improvement in performance of high self-controllers under induction conditions, as compared to baseline, by the higher self-reflection ability that accompanies high self-control. Specifically, a situation that is normally "hot" for high self-controllers is cooled through an induction that draws their attention to their high baseline self-control and accompanying positive affect. As a result, they reflect on their choices to a greater extent and act more in line with their usual optimal decision making ability. We thus both identify a specific environment where high self-control can prove to be a limiting factor for optimal decision making, and suggest a possible way to remedy that limitation, by providing a cooling period and drawing the attention of high self-controllers to the reasons for their sub-optimal strategy (namely, their positive feelings and high opinion of their own self-control). Together, the findings provide tantalizing implications for the sub-optimal market choices that even the most intelligent and successful individuals will make under the right conditions--and equally tantalizing ways to make those choices more sound

NOD2 Investigating IBD with Autophagy and Interleukins

Inflammatory bowel disease (IBD) is a chronic condition that causes inflammation and swelling in the digestive tract. Although two types of IBD exist, Crohn\u27s disease (CD) and Ulcerative Colitis, this review will focus mainly on CD. The common pathology in IBD is the induction of interleukins and an abnormal Paneth cell phenotype. CD is caused by environmental and multigenic factors, including mutations in NOD2 and RUNX-3. NOD2 promotes the induction of specific antimicrobial peptides that strengthen the immune system\u27s response against antigens. Mutations in NOD2 cause an overexpression of NF-kB activity and IL-1-ß processing, which increases susceptibility to CD. Deletion of RUNX-3 in mice induces colitis and causes an increase in certain interleukins. Moreover, IL-23R induces a pro-inflammatory response while IL-11R promotes an anti-inflammatory response. Defective autophagy has been linked to abnormal Paneth cells and an endotoxin-induced inflammatory response in mice. The most promising CD treatments involve procedures that reduce inflammation by decreasing interleukin levels. Specifically, injection of anti-interleukin 12 antibodies, increasing the production of glucocorticoids through LRH-1, and the addition of polysaccharide A (PSA) can all serve as possible treatments for CD by down-regulating the overactive immune system. Identifying more genes that increase susceptibility to CD can lead to novel treatments in the future

Long-term and rapid variability of the radio source J1603+1105

© 2017, Pleiades Publishing, Ltd. We present the long-term light curve of the radio source J1603+1105 and results of the study of its variability on timescales from several days to several weeks. From 2007, a flare with the maximum in 2010 was observed for the object that earlier showed no significant variations of flux density. Three flares with a successively decreasing amplitude were detected at an active phase in the long-term light curve. The characteristic time of the first one was 2.5 yrs. In five sets of daily observations of 95 to 120 days, the flux density variability on scales from 9 to 32 days in 2011, 2012, 2015, and 2016 was detected; in 2015 it was detected at three frequencies simultaneously. In 2011, the variability was found at a single frequency of 4.8 GHz; in 2012—at two frequencies, 4.8 and 7.7 GHz; in 2015—at 4.6, 8.2, and 11.2 GHz.We present instant spectra of the source at different flare phases showing that the dynamics of the flare development is consistent with the model, in which the variability is the result of the shock wave evolution in the radio source jet

Flux density variability of radio sources at declinations 10°-12°30′ (J2000) on time scales less than a month

Results of a search for and study of variability in a complete sample of flat-spectrum radio sources (83 objects) on time scales longer than a day are reported. The data were obtained in six series of daily observations on the RATAN-600 radio telescope made over 77-103 days at six frequencies from 0.97 to 21.7 GHz and at declinations of 10°-12°30′ (J2000). Variability on time scales of 3-30 days with significance levels below 1% was detected for 19 sources. The time scales, modulation indices, and spectra of the variability derived from an analysis of the light curves, structure functions, and autocorrelation functions are presented for these sources. For a number of them, intrinsic variability and extrinsic variability due to scintillations in the turbulent interstellar medium have been separated. The obtained source characteristics are compared with those for sources at declinations 4°-6° (B1950). © 2013 Pleiades Publishing, Ltd

Familial Parkinson's Disease Mutant E46K α-Synuclein Localizes to Membranous Structures, Forms Aggregates, and Induces Toxicity in Yeast Models

In Parkinson's disease (PD), midbrain dopaminergic neuronal death is linked to the accumulation of aggregated α-synuclein. The familial PD mutant form of α-synuclein, E46K, has not been thoroughly evaluated yet in an organismal model system. Here, we report that E46K resembled wild-type (WT) α-synuclein in Saccharomyces cerevisiae in that it predominantly localized to the plasma membrane, and it did not induce significant toxicity or accumulation. In contrast, in Schizosaccharomyces pombe, E46K did not associate with the plasma membrane. Instead, in one strain, it extensively aggregated in the cytoplasm and was as toxic as WT. Remarkably, in another strain, E46K extensively associated with the endomembrane system and was more toxic than WT. Our studies recapitulate and extend aggregation and phospholipid membrane association properties of E46K previously observed in vitro and cell culture. Furthermore, it supports the notion that E46K generates toxicity partly due to increased association with endomembrane systems within cells

Long-term variability of the radio source J0010+1058 in 2000–2013

© 2015, Pleiades Publishing, Ltd. During thirteen-year monitoring of the source J0010+1058, four bursts have been observed with an amplitude greater than 1 Jy on a frequency of 21.7 GHz. Using autocorrelation functions, we determined the average characteristic burst time τacf ≈ 1.55 ± 0.1 yr (max-min), identical at five frequencies: 2.3, 4.8, 7.7, 11.2, and 21.7 GHz, which provides the linear sizes of the emission region R ≈ cτacf ≈ 0.48 pc, and the angular ones—0.28 mas; the brightness temperature is 0.6–6.5 × 1011 K at the frequencies 21.7–2.3 GHz. Moreover, at frequencies higher than 2.3 GHz, there is one more characteristic time τ ≈ 0.6 yr. We estimated the average lag time of the bursts in relation to a frequency of 21.7 GHz as 150, 210, 270, and 390 days at 11.2, 7.7, 4.8, and 2.3 GHz respectively, and some other source characteristics. Spectra obtained in different periods of source activity confirm the model of the burst development as a result of the evolution of a shock wave propagating along the radio source jet

Contribution of Alanine-76 and Serine Phosphorylation in α-Synuclein Membrane Association and Aggregation in Yeasts

In Parkinson's disease (PD), misfolded and aggregated α-synuclein protein accumulates in degenerating midbrain dopaminergic neurons. The amino acid alanine-76 in α-synuclein and phosphorylation at serine-87 and serine-129 are thought to regulate its aggregation and toxicity. However, their exact contributions to α-synuclein membrane association are less clear. We found that α-synuclein is indeed phosphorylated in fission yeast and budding yeast, the two models that we employed for assessing α-synuclein aggregation and membrane association properties, respectively. Surprisingly, blocking serine phosphorylation (S87A, S129A, and S87A/S129A) or mimicking it (S87D, S129D) altered α-synuclein aggregation in fission yeast. Either blocking or mimicking this phosphorylation increased endomembrane association in fission yeast, but only mimicking it decreased plasma membrane association in budding yeast. Polar substitution mutations of alanine-76 (A76E and A76R) decreased α-synuclein membrane association in budding yeast and decreased aggregation in fission yeast. These yeast studies extend our understanding of serine phosphorylation and alanine-76 contributions to α-synuclein aggregation and are the first to detail their impact on α-synuclein's plasma membrane and endomembrane association

Flux-density variability of the blazar S5 1803+784 (J1800+7828) on a timescale of a month

The variability of the blazar S5 1803+784 (J1800+7828) on a timescale of a month is analyzed using daily RATAN-600 observations in 2009 (a total of 154 observations) at five frequences from 2.3 to 21.7 GHz. Cyclic variability of the flux density was detected at 7.7, 11.1, and 21.7 GHz on a timescale of 34-35 days, with modulation indices of 2.1, 3.6, and 6.6%, respectively. Characteristic time scales are derived from the light curves and the structure and autocorrelation functions. The spectrum of the variable component is rising, with spectral index α ≈ 1.3. The delays of the light-curve maxima between 21.7-11.1 and 11.1-7.7 GHz are three to four days. The integrated spectra for different light-curve phases indicate that the maximum shifts toward lower frequencies as the flux density passes through the maximum. Our results suggest that the variability can be explained mainly by non-stationary processes in the radio source itself, due to the propagation of shocks in the jet. © 2013 Pleiades Publishing, Ltd

Spectra and variability of a sample of polar sources

The results of 154 daily observations of 33 sources in the declination interval 70°-84.° 5 (J 2000), made in 2009, are reported. Four objects are found to exhibit variations with typical time scales ranging from 8 to 35 days and modulation indices 2.1-5.6%. The spectra of the variable components are obtained. The same sources were observed again after six months, in 2010, for a duration of up to 55 days. The 11.1 GHz flux densities of one third of the sources varied by more than 10% between the two data sets. © 2013 Pleiades Publishing, Ltd