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Phishing is the spoofing of Internet websites or emails aimed at tricking users into entering sensitive information, with such goals as financial or identity theft. The current study sought to determine whether age is associated with increased susceptibility to phishing and whether tests of executive functioning can predict phishing susceptibility. A total of 193 cognitively intact participants, 91 younger adults and 102 older adults, were primarily recruited through a Psychology department undergraduate subject pool and a gerontology research registry, respectively. The Executive Functions Module from the Neuropsychological Assessment Battery and the Iowa Gambling Task were the primary cognitive predictors of reported phishing suspiciousness. Other predictors included age group (older vs. younger), sex, education, race, ethnicity, prior knowledge of phishing, prior susceptibility to phishing, and whether or not browsing behaviors were reportedly different in the laboratory setting versus at home. A logistic regression, which accounted for a 22.7% reduction in error variance compared to the null model and predicted phishing suspiciousness with 73.1% (95% CI [66.0, 80.3]) accuracy, revealed three statistically significant predictors: the main effect of education (b = 0.58, SE = 0.27) and the interactions of age group with prior awareness of phishing (b = 2.31, SE = 1.12) and performance on the Neuropsychological Assessment Battery Mazes test (b = 0.16, SE = 0.07). Whether or not older adults reported being suspicious of the phishing attacks used in this study was partially explained by educational history and prior phishing knowledge. This suggests that simple educational interventions may be effective in reducing phishing vulnerability. Although one test of executive functioning was found useful for identifying those at risk of phishing susceptibility, four tests were not found to be useful; these results speak to the need for more ecologically valid tools in clinical neuropsychology.

The literature on team cooperation has neglected the effects of relative kindness intention on cooperation, which we measure by comparing the kindness intentions of an agent to her group members to the kindness shown by other members to this same agent. We argue that the agent's emotional reaction to material payoff inequity is not constant, but rather affected by her relative kindness intention. Then, we apply the model to team projects with multiple partners and investigate how inequity-aversion and relative kindness intention jointly influence team cooperation. We first consider the case of homogeneous agents, where their marginal productivity levels and technical capacities are the same, and then consider the case of heterogeneous agents, where their marginal productivity levels and technical capacities are not the same. Our results show that inequity-aversion has no effect on effort expenditure in the former case, but does affect it in the latter case. The consideration of relative kindness intention may impact the agents' optimal cooperative effort expenditure when their technical capacities are different. In addition, it is beneficial for team cooperation, and might not only reduce the negative impact but also enhance the positive impact of inequity-aversion on the agents' effort expenditures.

BackgroundReactive nitrogen species (RNS) derived from dietary and salivary inorganic nitrogen oxides foment innate host defenses associated with the acidity of the stomach. The mechanisms by which these reactive species exert antimicrobial activity in the gastric lumen are, however, poorly understood.Methodology/principal findingsThe genetically tractable acid tolerance response (ATR) that enables enteropathogens to survive harsh acidity was screened for signaling pathways responsive to RNS. The nitric oxide (NO) donor spermine NONOate derepressed the Fur regulon that controls secondary lines of resistance against organic acids. Despite inducing a Fur-mediated adaptive response, acidified RNS largely repressed oral virulence as demonstrated by the fact that Salmonella bacteria exposed to NO donors during mildly acidic conditions were shed in low amounts in feces and exhibited ameliorated oral virulence. NO prevented Salmonella from mounting a de novo ATR, but was unable to suppress an already functional protective response, suggesting that RNS target regulatory cascades but not their effectors. Transcriptional and translational analyses revealed that the PhoPQ signaling cascade is a critical ATR target of NO in rapidly growing Salmonella. Inhibition of PhoPQ signaling appears to contribute to most of the NO-mediated abrogation of the ATR in log phase bacteria, because the augmented acid sensitivity of phoQ-deficient Salmonella was not further enhanced after RNS treatment.Conclusions/significanceSince PhoPQ-regulated acid resistance is widespread in enteric pathogens, the RNS-mediated inhibition of the Salmonella ATR described herein may represent a common component of innate host defenses.

BACKGROUND: Studies show that poststroke depression (PSD) increases mortality risk at 1 year. However, whether PSD increases the risk of recurrent stroke at 1 year remains unclear. This study was to investigate whether PSD at 2 weeks following a stroke could increase risk of recurrent stroke at 1 year. METHODS AND RESULTS: This was a multi-centered prospective cohort study. A total of 2306 patients with acute stroke were enrolled in our study. PSD was diagnosed according to the criteria set by the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV). The outcomes of recurrent stroke were followed up via face-to-face or phone interview. A total of 1713 patients had complete follow-up data, with 481 (28.1%) cases of PSD and 158 (9.2%) cases of cumulative recurrent stroke at 1 year. Multivariate logistic regression analysis showed a 49% increase of OR of recurrent stroke at 1 year in patients with PSD, compared to patients without PSD following a stroke (OR=1.49, 95%CI: 1.03-2.15). There was no significant correlation between anti-depressant drugs and the risk of recurrent stroke at 1 year following a stroke (OR=1.96, 95%: CI 0.95-4.04). CONCLUSIONS: Based on the DSM-IV diagnostic criteria, nearly 3 out of 10 hospitalized stroke patients in China were diagnosed with PSD at 2 weeks following a stroke. PSD is associated with a higher risk of recurrent stroke at 1 year. Our study did not find benefit of anti-depressant drugs in reducing such risk.

A multivariate linear regression model was proposed to achieve short period prediction of PM2.5 (fine particles with an aerodynamic diameter of 2.5 μm or less). The main parameters for the proposed model included data on aerosol optical depth (AOD) obtained through remote sensing, meteorological factors from ground monitoring (wind velocity, temperature, and relative humidity), and other gaseous pollutants (SO2, NO2, CO, and O3). Beijing City was selected as a typical region for the case study. Data on the aforementioned variables for the city throughout 2015 were used to construct two regression models, which were discriminated by annual and seasonal data, respectively. The results indicated that the regression model based on annual data had (R2 = 0.766) goodness-of-fit and (R2 = 0.875) cross-validity. However, the regression models based on seasonal data for spring and winter were more effective, achieving 0.852 and 0.874 goodness-of-fit, respectively. Model uncertainties were also given, with the view of laying the foundation for further study. [ABSTRACT FROM AUTHOR]

Chromodomain helicase DNA binding protein 5 (CHD5) was previously proposed to function as a potent tumor suppressor by acting as a master regulator of a tumor-suppressive network. CHD5 is down-regulated in several cancers, including leukemia and is responsible for tumor generation and progression. However, the mechanism of CHD5 down-regulation in leukemia is largely unknown. In this study, quantitative reverse-transcriptase polymerase chain reaction and western blotting analyses revealed that CHD5 was down-regulated in human leukemia cell lines and samples. Luciferase reporter assays showed that most of the baseline regulatory activity was localized from 500 to 200 bp upstream of the transcription start site. Bisulfite DNA sequencing of the identified regulatory element revealed that the CHD5 promoter was hypermethylated in human leukemia cells and samples. Thus, CHD5 expression was inversely correlated with promoter DNA methylation in these samples. Treatment with DNA methyltransferase inhibitor 5-aza-2′-deoxycytidine (DAC) activates CHD5 expression in human leukemia cell lines. In vitro luciferase reporter assays demonstrated that methylation of the CHD5 promoter repressed its promoter activity. Furthermore, a chromatin immunoprecipitation assay combined with qualitative PCR identified activating protein 2 (AP2) as a potential transcription factor involved in CHD5 expression and indicated that treatment with DAC increases the recruitment of AP2 to the CHD5 promoter. In vitro transcription-factor activity studies showed that AP2 over-expression was able to activate CHD5 promoter activity. Our findings indicate that repression of CHD5 gene expression in human leukemia is mediated in part by DNA methylation of its promoter. [ABSTRACT FROM AUTHOR]