The influence of societal individualism on a century of tobacco use: modelling the prevalence of smoking

Smoking of tobacco is predicted to cause approximately six million deaths worldwide in 2014. Responding effectively to this epidemic requires a thorough understanding of how smoking behaviour is transmitted and modified. Here, we present a new mathematical model of the social dynamics that cause cigarette smoking to spread in a population. Our model predicts that more individualistic societies will show faster adoption and cessation of smoking. Evidence from a new century-long composite data set on smoking prevalence in 25 countries supports the model, with direct implications for public health interventions around the world. Our results suggest that differences in culture between societies can measurably affect the temporal dynamics of a social spreading process, and that these effects can be understood via a quantitative mathematical model matched to observations

Autophagy occurs upstream or parallel to the apoptosome during histolytic cell death

Histolysis refers to a widespread disintegration of tissues that is morphologically distinct from apoptosis and often associated with the stimulation of autophagy. Here, we establish that a component of the apoptosome, and pivotal regulator of apoptosis, is also required for histolytic cell death. Using in vivo and ex vivo assays, we demonstrate a global apoptogenic requirement for dark, the fly ortholog of Apaf1, and show that a required focus of dark– organismal lethality maps to the central nervous system. We further demonstrate that the Dark protein itself is a caspase substrate and find that alterations of this cleavage site produced the first hypermorphic point mutation within the Apaf1/Ced-4 gene family. In a model of ‘autophagic cell death’, dark was essential for histolysis but dispensable for characteristic features of the autophagic program, indicating that the induction of autophagy occurs upstream or parallel to histolytic cell death. These results demonstrate that stimulation of autophagy per se is not a ‘killing event’ and, at the same time, establish that common effector pathways, regulated by the apoptosome, can underlie morphologically distinct forms of programmed cell death

Overexpression screen of interferon-stimulated genes identifies RARRES3 as a restrictor of Toxoplasma gondii infection

Toxoplasma gondii is an important human pathogen infecting an estimated one in three people worldwide. The cytokine interferon gamma (IFNγ) is induced during infection and is critical for restricting T. gondii growth in human cells. Growth restriction is presumed to be due to the induction of interferon-stimulated genes (ISGs) that are upregulated to protect the host from infection. Although there are hundreds of ISGs induced by IFNγ, their individual roles in restricting parasite growth in human cells remain somewhat elusive. To address this deficiency, we screened a library of 414 IFNγ induced ISGs to identify factors that impact T. gondii infection in human cells. In addition to IRF1, which likely acts through the induction of numerous downstream genes, we identified RARRES3 as a single factor that restricts T. gondii infection by inducing premature egress of the parasite in multiple human cell lines. Overall, while we successfully identified a novel IFNγ induced factor restricting T. gondii infection, the limited number of ISGs capable of restricting T. gondii infection when individually expressed suggests that IFNγ-mediated immunity to T. gondii infection is a complex, multifactorial process

Solar Carbon Monoxide, Thermal Profiling, and the Abundances of C, O, and their Isotopes

A solar photospheric "thermal profiling" analysis is presented, exploiting the infrared rovibrational bands of carbon monoxide (CO) as observed with the McMath-Pierce Fourier transform spectrometer (FTS) at Kitt Peak, and from above the Earth's atmosphere by the Shuttle-borne ATMOS experiment. Visible continuum intensities and center-limb behavior constrained the temperature profile of the deep photosphere, while CO center-limb behavior defined the thermal structure at higher altitudes. The oxygen abundance was self consistently determined from weak CO absorptions. Our analysis was meant to complement recent studies based on 3-D convection models which, among other things, have revised the historical solar oxygen (and carbon) abundance downward by a factor of nearly two; although in fact our conclusions do not support such a revision. Based on various considerations, an oxygen abundance of 700+/-100 ppm (parts per million relative to hydrogen) is recommended; the large uncertainty reflects the model sensitivity of CO. New solar isotopic ratios also are reported for 13C, 17O, and 18O.Comment: 90 pages, 19 figures (some with parts "a", "b", etc.); to be published in the Astrophysical Journal Supplement

Membership role and subjective group dynamics: Impact on evaluative intragroup differentiation and commitment to prescriptive norms

Two studies examined participants’ evaluations of ingroup or outgroup normative and deviant members and changes in agreement with a prescriptive norm. In Experiment 1 (N = 51), the normative target was either a full or marginal ingroup or outgroup member, and the deviant was a full member. In Experiment 2 (N = 113), both targets were full or marginal members, or one was a full member and the other was marginal. As predicted, maximal upgrading of normative members and downgrading of deviant members, as well as endorsement of the norm, occurred when both targets were full ingroup members. In contrast, the deviant was derogated least and the deviant’s position was endorsed most when the deviant target was a full ingroup member and the normative target was a marginal ingroup member. Evaluations of normative and deviant ingroup members mediated the effects of their role on participants’ agreement with the norm

A collective form of cell death requires homeodomain interacting protein kinase

We examined post-eclosion elimination of the Drosophila wing epithelium in vivo where collective “suicide waves” promote sudden, coordinated death of epithelial sheets without a final engulfment step. Like apoptosis in earlier developmental stages, this unique communal form of cell death is controlled through the apoptosome proteins, Dronc and Dark, together with the IAP antagonists, Reaper, Grim, and Hid. Genetic lesions in these pathways caused intervein epithelial cells to persist, prompting a characteristic late-onset blemishing phenotype throughout the wing blade. We leveraged this phenotype in mosaic animals to discover relevant genes and establish here that homeodomain interacting protein kinase (HIPK) is required for collective death of the wing epithelium. Extra cells also persisted in other tissues, establishing a more generalized requirement for HIPK in the regulation of cell death and cell numbers